RNA-Seq analysis miR-455-3p overexpression effect on breast cancer cell line
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ABSTRACT:
PROVIDER: PRJNA530241 | ENA |
REPOSITORIES: ENA
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Project description:MiR-455-3p has been reported to suppress the expression of ROCK2, HOXB5, hTERT, and RUNX2, which are involved in multiple biological processes including renal fibrosis, chondrogenic development and differentiation, Alzheimer’s disease, preeclampsia, and tumorigenesis. Here, we showed that miR-455-3p broadly inhibited TGF-beta-induced EMT by repressing the expression of Smad2, ZEB1, and HDAC2 in breast cancer cells, and that miR-455-3p loss-of-function promotes the acquisition of cell invasive properties and the ability to metastasize. These results indicate that miR-455-3p represents an important node that inhibits metastasis of breast cancer.
2019-09-06 | GSE129146 | GEO
Project description:Long non-coding RNAs (lncRNAs) play pivotal roles in diseases such as osteoarthritis (OA). However, knowledge of the biological roles of lncRNAs is limited in OA. We aimed to explore the biological function and molecular mechanism of HOTTIP in chondrogenesis and cartilage degradation. We used the human mesenchymal stem cell (MSC) model of chondrogenesis, in parallel with, tissue biopsies from normal and OA cartilage to detect HOTTIP, CCL3, and miR-455-3p expression in vitro. Biological interactions between HOTTIP and miR-455-3p were determined by RNA silencing and overexpression in vitro. We evaluated the effect of HOTTIP on chondrogenesis and degeneration, and its regulation of miR-455-3p via competing endogenous RNA (ceRNA). Our in vitro ceRNA findings were further confirmed within animal models in vivo. Mechanisms of ceRNAs were determined by bioinformatic analysis, a luciferase reporter system, RNA pull-down, and RNA immunoprecipitation (RIP) assays. We found reduced miR-455-3p expression and significantly upregulated lncRNA HOTTIP and CCL3 expression in OA cartilage tissues and chondrocytes. The expression of HOTTIP and CCL3 was increased in chondrocytes treated with interleukin-1β (IL-1β) in vitro. Knockdown of HOTTIP promoted cartilage-specific gene expression and suppressed CCL3. Conversely, HOTTIP overexpression reduced cartilage-specific genes and increased CCL3. Notably, HOTTIP negatively regulated miR-455-3p and increased CCL3 levels in human primary chondrocytes. Mechanistic investigations indicated that HOTTIP functioned as ceRNA for miR-455-3p enhanced CCL3 expression. Taken together, the ceRNA regulatory network of HOTTIP/miR-455-3p/CCL3 plays a critical role in OA pathogenesis and suggests HOTTIP is a potential target in OA therapy.
2019-08-12 | PXD014988 | Pride
Project description:Overexpression of miR-127-3p in LN229 glioblastoma cells promotes their migration and invasion in vitro and in vivo in xenograft models. We used microarrays to detail the global programme of gene expression in miR-127-3p overexpression LN229 cells compared with mock overexpression LN229 cells MiR-127-3p overexpression LN229 cells and and mock overexpression LN229 cells were cultured in DMEM cell culture media for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain the genes regulated by miR-127-3p in glioblastoma cell lines.
2014-09-01 | E-GEOD-50173 | biostudies-arrayexpress
Project description:This is a prospective-retrospective study to determine if the expression of the miRNA’s miR-31-3p and miR-31-5p are prognostic of patient outcomes or predictive of the benefit from anti-EGFR therapy in stage III Colon Cancer. The present study will utilize FFPE tumor samples collected from patients enrolled in the PETACC-8 study conducted by the Fédération Francophone de Cancérologie Digestive (FFCD). This phase 3 clinical trial prospectively randomized fully resected stage III colon cancer patients to receive adjuvant treatment with either FOLFOX-4 plus cetuximab or FLOFOX-4 alone.
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Project description:Oxaliplatin (oxPt) resistance in colorectal cancers (CRC) is a major unsolved problem. Consequently, predictive markers and a better understanding of resistance mechanisms are urgently needed. To investigate if the recently identified predictive miR-625-3p is functionally involved in oxPt resistance, stable and inducible models of miR-625-3p dysregulation were analyzed. Ectopic expression of miR-625-3p in CRC cells led to increased resistance towards oxPt. The mitogen-activated protein kinase (MAPK) kinase 6 (MAP2K6/MKK6) – an activator of p38 MAPK - was identified as a functional target of miR-625-3p, and, in agreement, was down-regulated in patients not responding to oxPt therapy. The miR-625-3p resistance phenotype could be reversed by anti-miR-625-3p treatment and by ectopic expression of a miR-625-3p insensitive MAP2K6 variant. Transcriptome, proteome and phosphoproteome profiles revealed inactivation of MAP2K6-p38 signaling as a possible driving force behind oxPt resistance. We conclude that miR-625-3p induces oxPt resistance by abrogating MAP2K6-p38 regulated apoptosis and cell cycle control networks.
2017-03-29 | MSV000080762 | MassIVE
Project description:Overexpression of miR-127-3p in LN229 glioblastoma cells promotes their migration and invasion in vitro and in vivo in xenograft models. We used microarrays to detail the global programme of gene expression in miR-127-3p overexpression LN229 cells compared with mock overexpression LN229 cells
2014-09-01 | GSE50173 | GEO
Project description:Primary cilium serves as a cellular M-bM-^@M-^\antennaM-bM-^@M-^] to sense environmental signals. Ciliogenesis requires the removal of CP110 to convert the mother centriole into the basal body. Actin dynamics is also critical for cilia formation. How these distinct processes are properly regulated remains unknown. Here we show that miR-129-3p, a microRNA conserved in the vertebrates, controlled cilia assembly by down-regulating both CP110 and four proteins critical for actin dynamics, Arp2, Toca1, abLIM1, and abLIM3. Consistently, blocking miR-129-3p repressed cilia formation in cultured mammalian cells, whereas its overexpression potently induced ciliogenesis in proliferating cells and extraordinary cilia elongation. Moreover, inhibition of miR-129-3p in zebrafish embryos suppressed cilia assembly in the KupfferM-bM-^@M-^Ys vesicle and pronephric duct, leading to developmental abnormalities including curved body, pericardial oedema, and randomised left-right patterning. Our results thus unravel a novel mechanism that orchestrates both the centriole-to-basal body transition and subsequent cilia assembly via microRNA-mediated posttranscriptional regulations. We want to find the targets of miR-129-3p by overexpressing miR-129-3p oligo or control oligo in hTERT-RPE1 cells. Through microarray analysis we could check the downregulated genes and these genes might be the targets of miR-129-3p. RPE1 cells were transfected with control (Ctrl) or miR-129-3p (M129) oligo for 72h, and harvested for RNA extraction and hybridization on Affymetrix microarrays. Two samples: RPE1-Ctrl, RPE1-M129
2012-05-31 | E-GEOD-34846 | biostudies-arrayexpress
Project description:Effect of miR-200c-3p overexpression on primary human macrophages
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Project description:Analysis of the effect of the miRNA set (miR-32/455/181a/181b) on global gene expression. The hypothesis tested was that overexpression of these miRNAs would produce changes in gene expression similar to changes caused by PI3K knockdown. Data provided insight into genes that are disrupted with either individual miRNA and siRNA or the combination of miRNAs or siRNAs.
2012-12-29 | GSE43195 | GEO
Project description:Analysis of the effect of the miRNA set (miR-32/455/181a/181b) on global gene expression. The hypothesis tested was that overexpression of these miRNAs would produce changes in gene expression similar to changes caused by PI3K knockdown. Data provided insight into genes that are disrupted with either individual miRNA and siRNA or the combination of miRNAs or siRNAs. Total RNA was isolated from KYSE30 cells transfected with either miRNA or siRNA for global expression analysis.
2012-12-29 | E-GEOD-43195 | biostudies-arrayexpress